Early life multiple exposures and child cognitive function: A multi-centric birth cohort study in six European countries

Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old,...

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Vydáno v:	Environmental pollution (1987) Ročník 284; s. 117404
Hlavní autoři:	Julvez, Jordi, López-Vicente, Mónica, Warembourg, Charline, Maitre, Lea, Philippat, Claire, Gützkow, Kristine B., Guxens, Monica, Evandt, Jorunn, Andrusaityte, Sandra, Burgaleta, Miguel, Casas, Maribel, Chatzi, Leda, de Castro, Montserrat, Donaire-González, David, Gražulevičienė, Regina, Hernandez-Ferrer, Carles, Heude, Barbara, Mceachan, Rosie, Mon-Williams, Mark, Nieuwenhuijsen, Mark, Robinson, Oliver, Sakhi, Amrit K., Sebastian-Galles, Nuria, Slama, Remy, Sunyer, Jordi, Tamayo-Uria, Ibon, Thomsen, Cathrine, Urquiza, Jose, Vafeiadi, Marina, Wright, John, Basagaña, Xavier, Vrijheid, Martine
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England Elsevier Ltd 01.09.2021 Elsevier Elsevier Applied Science Publishers
Témata:	alcohol drinking algorithms Birth cohort study Chemical biomarkers Child child nutrition childhood children Cognition Cohort Studies Environmental epidemiology Environmental Exposure Europe Exposome fast foods Female food intake Humans indoor air pollution Life Sciences memory mercury meteorology Neurodevelopment Neuropsychological development organic foods perfluorooctane sulfonic acid Pregnancy Santé publique et épidémiologie second hand smoke traffic Europe Environmental epidemiology Neurodevelopment Exposome Chemical biomarkers Birth cohort study Neuropsychological development
ISSN:	0269-7491, 1873-6424, 1873-6424
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Abstract	Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (−1.25; −2.10, −0.40), house crowding (−0.39; −0.62, −0.16), and child environmental tobacco smoke (ETS) (−0.89; −1.42, −0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (−0.09; −0.16, −0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. [Display omitted] •Previous evidence for environmental risk factor associations with neurodevelopment is based on analyses of single exposures.•We systematically analysed multiple environmental exposures in relation to child neurodevelopment.•The findings describe a list of outcome-related exposures: Diet, house crowding, indoor air pollution and tobacco smoke.•The findings show methodological complexities of analysing multiple exposures and their associations with neurodevelopment.
AbstractList	Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6-11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (-1.25; -2.10, -0.40), house crowding (-0.39; -0.62, -0.16), and child environmental tobacco smoke (ETS) (-0.89; -1.42, -0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (-0.09; -0.16, -0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality.Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6-11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (-1.25; -2.10, -0.40), house crowding (-0.39; -0.62, -0.16), and child environmental tobacco smoke (ETS) (-0.89; -1.42, -0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (-0.09; -0.16, -0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (−1.25; −2.10, −0.40), house crowding (−0.39; −0.62, −0.16), and child environmental tobacco smoke (ETS) (−0.89; −1.42, −0.35), were all associated with lower CPM scores. Indoor PM₂.₅ exposure was associated with lower N-Back scores (−0.09; −0.16, −0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6-11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (-1.25; -2.10, -0.40), house crowding (-0.39; -0.62, -0.16), and child environmental tobacco smoke (ETS) (-0.89; -1.42, -0.35), were all associated with lower CPM scores. Indoor PM exposure was associated with lower N-Back scores (-0.09; -0.16, -0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (−1.25; −2.10, −0.40), house crowding (−0.39; −0.62, −0.16), and child environmental tobacco smoke (ETS) (−0.89; −1.42, −0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (−0.09; −0.16, −0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. [Display omitted] •Previous evidence for environmental risk factor associations with neurodevelopment is based on analyses of single exposures.•We systematically analysed multiple environmental exposures in relation to child neurodevelopment.•The findings describe a list of outcome-related exposures: Diet, house crowding, indoor air pollution and tobacco smoke.•The findings show methodological complexities of analysing multiple exposures and their associations with neurodevelopment. Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal and childhood environmental exposures and cognition. The study sample included data of 1298 mother-child pairs, children were 6–11 years-old, from six European birth cohorts. We measured 87 exposures during pregnancy and 122 cross-sectionally during childhood, including air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals and life styles. The measured cognitive domains were fluid intelligence (Raven's Coloured Progressive Matrices test, CPM), attention (Attention Network Test, ANT) and working memory (N-Back task). We used two statistical approaches to assess associations between exposure and child cognition: the exposome-wide association study (ExWAS) considering each exposure independently, and the deletion-substitution-addition algorithm (DSA) considering all exposures simultaneously to build a final multiexposure model. Based on this multiexposure model that included the exposure variables selected by ExWAS and DSA models, child organic food intake was associated with higher fluid intelligence (CPM) scores (beta = 1.18; 95% CI = 0.50, 1.87) and higher working memory (N-Back) scores (0.23; 0.05, 0.41), and child fast food intake (−1.25; −2.10, −0.40), house crowding (−0.39; −0.62, −0.16), and child environmental tobacco smoke (ETS) (−0.89; −1.42, −0.35), were all associated with lower CPM scores. Indoor PM2.5 exposure was associated with lower N-Back scores (−0.09; −0.16, −0.02). Additional associations in the unexpected direction were found: Higher prenatal mercury levels, maternal alcohol consumption and child higher perfluorooctane sulfonic acid (PFOS) levels were associated with better cognitive performance; and higher green exposure during pregnancy with lower cognitive performance. This first comprehensive and systematic study of many prenatal and childhood environmental risk factors suggests that unfavourable child nutrition, family crowdedness and child indoor air pollution and ETS exposures adversely and cross-sectionally associate with cognitive function. Unexpected associations were also observed and maybe due to confounding and reverse causality. Prenatal and childhood exposome-wide associations with child fluid intelligence (CPM). The exposures selected by Deletion-substitution-addition algorithm are represented by a triangle. Child fluid intelligence is mainly associated with childhood exposome, fast-food (negative association, left sided) and organic food consumption (positive, right sided), house crowding (negative, left sided), and child environmental tobacco smoke (ETS, negative, left sided). Image 1 • Previous evidence for environmental risk factor associations with neurodevelopment is based on analyses of single exposures. • We systematically analysed multiple environmental exposures in relation to child neurodevelopment. • The findings describe a list of outcome-related exposures: Diet, house crowding, indoor air pollution and tobacco smoke. • The findings show methodological complexities of analysing multiple exposures and their associations with neurodevelopment.
ArticleNumber	117404
Author	Urquiza, Jose Heude, Barbara Chatzi, Leda Donaire-González, David López-Vicente, Mónica Casas, Maribel Vrijheid, Martine Nieuwenhuijsen, Mark Warembourg, Charline Basagaña, Xavier Mceachan, Rosie Sebastian-Galles, Nuria Hernandez-Ferrer, Carles Vafeiadi, Marina Burgaleta, Miguel Wright, John Slama, Remy Sunyer, Jordi Gražulevičienė, Regina Philippat, Claire Andrusaityte, Sandra Sakhi, Amrit K. Evandt, Jorunn Robinson, Oliver Guxens, Monica Maitre, Lea de Castro, Montserrat Tamayo-Uria, Ibon Mon-Williams, Mark Gützkow, Kristine B. Julvez, Jordi Thomsen, Cathrine
Author_xml	– sequence: 1 givenname: Jordi orcidid: 0000-0003-0818-4003 surname: Julvez fullname: Julvez, Jordi email: jordi.julvez@iispv.cat organization: Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari Sant Joan de Reus, Reus (Tarragona), Catalonia, Spain – sequence: 2 givenname: Mónica surname: López-Vicente fullname: López-Vicente, Mónica organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 3 givenname: Charline orcidid: 0000-0003-2716-9167 surname: Warembourg fullname: Warembourg, Charline organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 4 givenname: Lea surname: Maitre fullname: Maitre, Lea organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 5 givenname: Claire surname: Philippat fullname: Philippat, Claire organization: Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences (IAB), Inserm U1209, CNRS UMR 5309, Université Grenoble Alpes, 38000, Grenoble, France – sequence: 6 givenname: Kristine B. surname: Gützkow fullname: Gützkow, Kristine B. organization: Department of Environmental Health, Norwegian Institute of Public Health, Oslo, Norway – sequence: 7 givenname: Monica surname: Guxens fullname: Guxens, Monica organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 8 givenname: Jorunn surname: Evandt fullname: Evandt, Jorunn organization: Department of Environmental Health, Norwegian Institute of Public Health, Oslo, Norway – sequence: 9 givenname: Sandra surname: Andrusaityte fullname: Andrusaityte, Sandra organization: Vytauto Didziojo Universitetas (VDU), Kaunus, Lithuania – sequence: 10 givenname: Miguel orcidid: 0000-0002-3974-9292 surname: Burgaleta fullname: Burgaleta, Miguel organization: Center for Brain and Cognition, Department of Technology, Universitat Pompeu Fabra, Roc Boronat 138, 08018, Barcelona, Catalonia, Spain – sequence: 11 givenname: Maribel surname: Casas fullname: Casas, Maribel organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 12 givenname: Leda surname: Chatzi fullname: Chatzi, Leda organization: Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece – sequence: 13 givenname: Montserrat orcidid: 0000-0001-6547-5953 surname: de Castro fullname: de Castro, Montserrat organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 14 givenname: David surname: Donaire-González fullname: Donaire-González, David organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 15 givenname: Regina surname: Gražulevičienė fullname: Gražulevičienė, Regina organization: Vytauto Didziojo Universitetas (VDU), Kaunus, Lithuania – sequence: 16 givenname: Carles orcidid: 0000-0002-8029-7160 surname: Hernandez-Ferrer fullname: Hernandez-Ferrer, Carles organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 17 givenname: Barbara orcidid: 0000-0002-1565-1629 surname: Heude fullname: Heude, Barbara organization: Université de Paris, Centre for Research in Epidemiology and Statistics (CRESS), INSERM, INRAE, Paris, France – sequence: 18 givenname: Rosie surname: Mceachan fullname: Mceachan, Rosie organization: Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – sequence: 19 givenname: Mark orcidid: 0000-0001-7595-8545 surname: Mon-Williams fullname: Mon-Williams, Mark organization: Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – sequence: 20 givenname: Mark surname: Nieuwenhuijsen fullname: Nieuwenhuijsen, Mark organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 21 givenname: Oliver orcidid: 0000-0002-4735-0468 surname: Robinson fullname: Robinson, Oliver organization: MRC Centre for Environment and Health, School of Public Health, Imperial College London, UK – sequence: 22 givenname: Amrit K. surname: Sakhi fullname: Sakhi, Amrit K. organization: Department of Environmental Health, Norwegian Institute of Public Health, Oslo, Norway – sequence: 23 givenname: Nuria surname: Sebastian-Galles fullname: Sebastian-Galles, Nuria organization: Center for Brain and Cognition, Department of Technology, Universitat Pompeu Fabra, Roc Boronat 138, 08018, Barcelona, Catalonia, Spain – sequence: 24 givenname: Remy surname: Slama fullname: Slama, Remy organization: Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences (IAB), Inserm U1209, CNRS UMR 5309, Université Grenoble Alpes, 38000, Grenoble, France – sequence: 25 givenname: Jordi surname: Sunyer fullname: Sunyer, Jordi organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 26 givenname: Ibon surname: Tamayo-Uria fullname: Tamayo-Uria, Ibon organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 27 givenname: Cathrine surname: Thomsen fullname: Thomsen, Cathrine organization: Department of Environmental Health, Norwegian Institute of Public Health, Oslo, Norway – sequence: 28 givenname: Jose orcidid: 0000-0003-2220-607X surname: Urquiza fullname: Urquiza, Jose organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 29 givenname: Marina surname: Vafeiadi fullname: Vafeiadi, Marina organization: Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece – sequence: 30 givenname: John orcidid: 0000-0001-9572-7293 surname: Wright fullname: Wright, John organization: Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – sequence: 31 givenname: Xavier surname: Basagaña fullname: Basagaña, Xavier organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain – sequence: 32 givenname: Martine orcidid: 0000-0002-7090-1758 surname: Vrijheid fullname: Vrijheid, Martine organization: Barcelona Institute for Global Health (ISGlobal), Barcelona, Catalonia, Spain
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Snippet	Epidemiological studies mostly focus on single environmental exposures. This study aims to systematically assess associations between a wide range of prenatal...
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SubjectTerms	alcohol drinking algorithms Birth cohort study Chemical biomarkers Child child nutrition childhood children Cognition Cohort Studies Environmental epidemiology Environmental Exposure Europe Exposome fast foods Female food intake Humans indoor air pollution Life Sciences memory mercury meteorology Neurodevelopment Neuropsychological development organic foods perfluorooctane sulfonic acid Pregnancy Santé publique et épidémiologie second hand smoke traffic
Title	Early life multiple exposures and child cognitive function: A multi-centric birth cohort study in six European countries
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